Interest in neuroendocrine function of depressives has disclosed several findings that appear to be consistent and reproducible during the acute phase of disease. These include: 1) hypersecretion of cortisol and "early escape" from dexamethasone suppression; 2) decreased growth hormone (HGH) and glucose responses to insulin-induced hypoglycemia; and 3) a diminished response of thyroid-stimulating hormone (TSH) to thyrotropin-releasing hormone (TRH) and an HGH response to TRH not present in normals. The cortisol abnormalities are usually normal after recovery from acute depression. The decreased HGH response to insulin tolerance testing and diminished response of TSH to TRH often persist after recovery in a portion of those demonstrating this finding. Recently, Schlesser, Winokur and Sherman were able to correlate nonsuppression after dexamethasone with the clinical categories of acute depression according to the genetic paradigm of Winokur. This was the first report of a distinct neuroendocrine abnormality supporting an objectively defined classification of unipolar illness. We propose that when the results of neuroendocrine perturbation tests are examined according to the genetic classification that consistent abnormalities may be found that were not apparent when responses were studied in a heterogeneous population. The purpose of this study is to retest the suppressors and nonsuppressors from previous neuroendocrine evaluation to determine whether there are continuing neuroendocrine abnormalities in the recovered phase that serve as markers for the depressive trait.